Dry Eye Disease (“DED”) is a condition that affects millions of people worldwide. More than 40 million people in North America have some form of dry eye, and many millions more suffer worldwide. DED results from the disruption of the natural tear film on the surface of the eye, and can result in ocular discomfort, visual disturbance, and a reduction in vision-related quality of life. Activities of daily living such as driving, computer use, housework, and reading have also been shown to be negatively impacted by DED. Patients with severe cases of DED are at risk for serious ocular health deficiencies such as corneal ulceration, and can experience a quality of life deficiency comparable to that of moderate-severe angina.
DED is progressive in nature, and fundamentally results from insufficient tear coverage on the surface of the eye. This poor tear coverage prevents healthy gas exchange and nutrient transport for the ocular surface, promotes cellular desiccation and creates a poor refractive surface for vision. Poor tear coverage typically results from: 1) insufficient aqueous tear production from the lacrimal glands (e.g. secondary to post-menopausal hormonal deficiency, auto-immune disease, LASIK surgery, etc.), and/or 2) excessive evaporation of aqueous tear resulting from dysfunction of the meibomian glands. Low tear volume causes a hyperosmolar environment that induces an inflamed state of the ocular surface. This inflammatory response induces apoptosis of the surface cells which in turn prevents proper distribution of the tear film on the ocular surface so that any given tear volume is rendered less effective. This initiates a vicious cycle where more inflammation can ensue causing more surface cell damage, etc. Additionally, the neural control loop, which controls reflex tear activation, is disrupted because the sensory neurons in the surface of the eye are damaged. As a result, fewer tears are secreted and a second vicious cycle develops that results in further progression of the disease (fewer tears cause nerve cell loss, which results in fewer tears, etc.).
Commonly assigned U.S. patent application Ser. No. 14/256,915, filed Apr. 18, 2014, and titled “NASAL STIMULATION DEVICES AND METHODS,” U.S. patent application Ser. No. 14/630,471, filed Feb. 24, 2015, and titled “POLYMER FORMULATIONS FOR NASOLACRIMAL STIMULATION,” U.S. patent application Ser. No. 14/809,109, filed Jul. 24, 2015, and titled “STIMULATION PATTERNS FOR TREATING DRY EYE,” and U.S. patent application Ser. No. 14/920,860, filed Oct. 22, 2015, and titled “STIMULATION DEVICES AND METHODS FOR TREATING DRY EYE,” each of which is hereby incorporated by reference in its entirety, describe devices and methods for application of electrical stimulation to sensory neurons in the nasal cavity to activate the nasolacrimal reflex and thereby increase tear production. However, it would be desirable to additionally supply a patient with a treatment recommendation for stimulus delivery.